This is part of a series which will review the history of why and how we are presently living with Darwinism and it will address why it matters. It is a historical overview and assessed in the light of to-day's scientific understanding of the deeper complexities of life...

 

Darwin wrote in a 27 May 1855 letter:
"if I really have as bad an expression, as my photograph gives me, how I can have one single friend is surprising."

John van Wyhe, ed. 2002-. The Complete Work of Charles Darwin Online (http://darwin-online.org.uk/)

CAMBRIDGE –ENGLAND – 1909
Darwin Celebrations
50 years since the publication of
‘On the Origin of Species’ & 100 years from his birth

Below is an excerpt taken from *Ronald Fisher’s notebook as quoted directly in AWF Edwards ‘Mathematizing Darwin’. (A. W. F. [Anthony] Edwards is one of Britain's most distinguished geneticists. He studied genetics at Cambridge as one of the last students of R. A. Fisher, and like Fisher he has contributed actively to both genetics and statistics)
*Ronald Fisher along with JBS Haldane, & Sewall Wright- Founders of the Modern Synthesis

“I first came to Cambridge in 1909, the year in which the centenary of Darwin’s birth and the jubilee of the publication of The Origin of Species were being celebrated. The new school of geneticists using Mendel’ s laws of inheritance was full of activity and confidence, and the shops were full of books good and bad from which one could see how completely many writers of this movement believed that Darwin’s position had been discredited”
Edwards (2011, 422).
http://link.springer.com/article/10.1007/s00265-010-1122-x

Source: postcard View of Sydney Street: Circa 1910; Photographer: Unknown; Publisher: W H Smith Kingsway series.http://www.keytothecity.co.uk/postcard.php?Id=57&CityId=15&From=Students

R. A. Fisher born 1890 – died 1962 age 72

Fisher is known as one of the three principal founders of population genetics, establishing a mathematical and statistical basis for biology and uniting natural selection with Mendelian genetics, and as one of the chief architects of the modern evolutionary synthesis.

A W F Edwards argues that Fisher’s close links to Darwin’s sons, meant that he had the means to Mathematize Darwin’s theory:

Abstract
Ernst Mayr called the first part of the evolutionary synthesis the ‘Fisherian synthesis’ on account of the dominant role played by R.A. Fisher in forging a mathematical theory of natural selection together with J.B.S. Haldane and Sewall Wright in the decade 1922–1932. It is here argued that Fisher’s contribution relied on a close reading of Darwin’s work to a much greater extent than did the contributions of Haldane and Wright, that it was synthetic in contrast to their analytic approach and that it was greatly influenced by his friendship with the Darwin family, particularly with Charles’s son Leonard....
http://link.springer.com/article/10.1007/s00265-010-1122-x

In another paper by AWF Edwards he states:

Richard Dawkins named him "the greatest biologist since Darwin. Not only was he the most original and constructive of the architects of the neo-Darwinian synthesis. Fisher also was the father of modern statistics and experimental design. He therefore could be said to have provided researchers in biology and medicine with their most important research tools, as well as with the modern version of biology's central theorem."
http://www.genetics.org/content/154/4/1419.full

Regarding the founders of the population genetics, Berkeley Education website state the following:[they]
“... showed how natural selection could operate in a Mendelian world. They carried out breeding experiments like previous geneticists, but they also did something new: they built sophisticated mathematical models of evolution.”
http://evolution.berkeley.edu/evolibrary/article/history_19

Who was Mendel and how was he so important in the modern synthesis?

Gregor Mendel wasn't the only one with an interest in heredity, and he wasn't the first to work with plants. So why were his results almost unknown until 1900 and the rediscovery of the laws of inheritance?
The common assumption is that Mendel was a monk working alone in a scientifically isolated atmosphere. His work was ignored because it was not widely distributed, and he didn't make an effort to promote himself. In actual fact, the reasons are more complex.
Mendel was part of the social and scientific circle of the time. He attended the University of Vienna, and came into contact with many prominent scientists. He had opportunities to travel to and attend scientific conferences. His paper, when published in 1865 in The Proceedings of the ...Natural Science Society, was exchanged with the publications of at least 120 other associations and societies, and was available in many libraries and scientific institutes. In addition, Mendel sent out 40 reprints to some of the most famous botanists at the time.
https://www.dnalc.org/view/16189-Biography-4-Gregor-Mendel-1822-1884-.html
In 'The Genetical Theory of Natural Selection'  A. W. F. Edwards (2000) states:

The Eclipse of Darwinism: It is difficult for us, as the century turns, to imagine the scepticism that surrounded Darwin's theory of evolution by natural selection 70 years ago and astonishing for us to recall that Mendelism itself was regarded in some quarters as antithetical to it.
http://www.genetics.org/content/154/4/1419.full

It is really not that astonishing if you review the history and even the views of more modern scientists regarding the very real issues embedded in not only Darwin's origial theory, but its genetically modified form. For instance, In 1914 Hugo De-Vries in  'THE PRINCIPLES OF THE THEORY OF MUTATION’:

...the basis, which the practice of artificial selection seemed to afford to the theory of natural selection, is a fallacious one, and that the idea of evolution by means of slow and imperceptible steps must therefore be abandoned.
— DeVries (1914, 80)
http://www.jstor.org/stable/1640345

The following excerpt below explains how de Vries and others were fully aware of Mendelian inheritence:

Hugo de Vries was born in Haarlem, Netherlands. He was a Professor of Botany at the University of Amsterdam when he began his genetic experiments with plants in 1880. He completed most of his hybridization experiments without knowing about Mendel's work. Based on his own results, de Vries drew the same conclusions as Mendel. De Vries published his work in 1900, first in French then in German. In the French report there was no mention of Mendel, but this was amended by de Vries in the German paper. It is possible that de Vries read Mendel's paper before he published his own, and included Mendel's name in the later printing when he realized that other people also knew about Mendel's work. De Vries may have thought that his own conclusions were superior to Mendel's.
... He observed that the original plant would occasionally have offspring with significant phenotypic differences such as leaf shape and plant sizes. Some of the offspring would pass the new "sport" (mutation) to their progeny; these de Vries designated as new species.
It is now known that de Vries had the right idea, but for the wrong reasons. Most of the variants that de Vries isolated from Oenothera lamarckiana were due to aberrant chromosomal segregations, and not to mutations associated with specific genes.
https://www.dnalc.org/view/16222-Biography-6-Hugo-de-Vries-1848-1935-.html

In other words, bringing Mendel’s inheritance laws into the picture did not automatically mean that the Neo-Darwinian version of genetic mutations (which are very different to the leaping evolutionary speciation observed by De vries) give it any validity. Nor did the natural selection problem ever go away even if it was dressed up in fancy population models and statistically mathematised to fit with Darwin’s theory and Mendel’s inheritance.
In a nut shell: De Vries’ theory and several other distinctly different theories, rejected gradualism and the idea of selection. For De Vries, gradualism was certainly not the way nature produced speces, as borne out by his years of studies and experiments. Furthermore, he argued that natural selection did not have the power to produce new and novel variations and in some cases was actually detrimental to evolving a new species. This is clearly documented in the review of De Vries’ Mutation Theory in the journal SCIENCE dating back to 1910:

It has long been recognized that natural selection really explains, not the origin of species, nor even the origin of adaptations, but the elimination of the unfit, and the persistence of adaptations; the fact that characters, both adaptive and non-adaptive, specific or not specific, must exist before they can be selected was previously well nigh lost sight of. The mutation-theory, then, seeks to account for “the origin of specific characters” (p. 211). In the second place, “Spontaneous variations are the facts on which this explanation is based” (p. 45), or, “We may express the essence of the mutation theory in the words: ‘Species have arisen after the manner of so-called spontaneous variations'” (p. 165). This marks the fundamental distinction between Darwinism and de Vriesism. … from the standpoint of the theory of mutation it is clear that the role played by natural selection in the origin of species is a destructive, and not a constructive one.” … Mutations are characterized first, by being entirely new features, “In contradistinction to fluctuating variations which are merely of a plus or minus character (p. 213); second, by the abruptness with which they appear, and third, by being transmitted by inheritance’ without selection. They arise suddenly and’ without any obvious cause; they increase and multiply because the new characters are inherited”
——   ‘Science’, (May 13^th 1910, p. 741)
http://www.jstor.org/stable/pdf/1634773.pdf?acceptTC=true

To find out just how right he was check out the following article:
http://diggingupthefuture.com/2015/08/10/part-two-if-it-didnt-happen-by-neo-darwinian-means-how-did-evolution-occur/
Our modern synthesis has consistently rejected leaps in complexity as a real fact of the fossil record. And Darwin’s species problem (how one species changes into another), remains unresolved as noted in ‘Resynthesizing Evolutionary and Developmental Biology’:

“The origin of species — Darwin’s problem — remains unsolved”
–  Gilbert, Opitz, and Raff (1996, 361)
http://www.evolbiol.ru/large_files/gilbert.pdf

See ‘Lamarck and the Sad Tale of the Blind Cave-Fish’ for more backgroud. https://www.smashwords.com/books/view/524805
(paperback version link) http://www.amazon.com/Lamarck-And-Tale-Blind-Cave-Fish/dp/178280465XI


Returning to De Vries, genetic mutations came to mean something entirely different to what De Vries had originally proposed. The modern synthesis now had a problem. If they had excluded any other means of changing a species, how was a species supposed to change? They did some experiments of genetic reshuffling of existing gene-pools of the same species and proposed that the only way to create genetic novelty (not employing De Vries’ ideas or any others who had demonstrate real, rapid and profound emergence of a new species) was to mathematically model the assumed rate of genetic mutations (mistakes in the copying process as genes are passed along the ancestral line) passed between populations, particularly those isolated and recombined gene-pools later down the line, and even though nobody ever seen a species change or become anything other than it was before (apart from some superficial type colour or variegated changes), they extrapolated this to all of evolution and based upon the assumption of direct ancestral relationships via linear descent from a common ancestor, attempted to demonstrate when one species gave rise to another (branching lineages and ancestral missing links were feverishly searched for) and calculated the timing of such assumed splits based upon the rate of genetic mutation (the molecular clock assumed to tick at the same rate for all species throughout evolution). Unfortunately, our ancestors may not be as common or related, at least not in the way we think and the genetic mutation (molecular) clock doesn’t appear to work that well:

DNA mutation clock proves tough to set

Geneticists meet to work out why the rate of change in the genome is so hard to pin down.

 In the past six years, more-direct measurements using ‘next-generation’ DNA sequencing have come up with quite different estimates. A number of studies have compared entire genomes of parents and their children — and calculated a mutation rate that consistently comes to about half that of the last-common-ancestor method.

A slower molecular clock worked well to harmonize genetic and archaeological estimates for dates of key events in human evolution, such as migrations out of Africa and around the rest of the world¹. But calculations using the slow clock gave nonsensical results when extended further back in time — positing, for example, that the most recent common ancestor of apes and monkeys could have encountered dinosaurs. Reluctant to abandon the older numbers completely, many researchers have started hedging their bets in papers, presenting multiple dates for evolutionary events depending on whether mutation is assumed to be fast, slow or somewhere in between. (Callaway in Nature 10^th March 2015)
http://www.nature.com/news/dna-mutation-clock-proves-tough-to-set-1.17079

 Furthermore, mutations don’t appear to bring about a new species, just deformed or dead things and population modelling used by the Neo-Darwinists has been described as numerology as seen in the following quotes by  LYNN MARGULIS

Neo-Darwinists say that new species emerge when mutations occur and modify an organism. I was taught over and over again that the accumulation of random mutations led to evolutionary change [which] led to new species. I believed it until I looked for evidence.-

— (Teresi 2011, 68) ‘Discover Magazine’ April edition

http://discovermagazine.com/2011/apr/16-interview-lynn-margulis-not-controversial-right

Mutations, in summary, tend to induce sickness, death, or deficiencies. No evidence in the vast literature of heredity changes shows unambiguous evidence that random mutation itself, even with geographical isolation of populations, leads to speciation.

 Margulis & Sagan (2008, 29) Acquiring Genomes: A Theory of the Origins of the Species

http://books.google.ie/books?id=DS-VehE00ncC&q=Mutations%2C+in+summary%2C+tend+to+induce+sickness%2C+death#v=snippet&q=Mutations%2C%20in%20summary%2C%20tend%20to%20induce%20sickness%2C%20death&f=false

When evolutionary biologists use computer modeling to find out how many mutations you need to get from one species to another, it’s not mathematics—it’s numerology.
Teresi (2011, 71) ‘Discover Magazine’ April edition

http://discovermagazine.com/2011/apr/16-interview-lynn-margulis-not-controversial-right
... Then how did one species evolve into another? This profound research question is assiduously undermined by the hegemony who flaunt their correct solution. Especially dogmatic are those molecular modelers of the tree of life who, ignorant of alternative topologies (such as webs), don't study ancestors.., they correlate computer code with names given by authorities to organisms they never see! Our zealous research, ever faithful to the god who dwells in the details, openly challenges such dogmatic certainty.
— Margulis (2006, 1) ‘The Phylogenetic Tree Topples’
https://www.americanscientist.org/issues/pub/2006/3/the-phylogenetic-tree-topples
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